Alpha-one antitrypsin (AAT) deficiency is a common autosomal co-dominant genetic disorder. This condition affects 1:2500 individuals of European ancestry, leading to the development of lung and liver disease. Within North American and Northern European populations, an estimated 4% of individuals are carriers of mutant alleles. AAT deficiency presents with an emphysema phenotype in the lungs of older subjects. AAT deficient subjects can also suffer from liver disease of varying severity; however, lung disease is the principle cause of death. AAT is a protease inhibitor predominantly synthesized in the liver that belongs to the serine protease inhibitor (serpin) family. Upon secretion into the blood stream, AAT enters the lungs where it inactivates excess neutrophil elastase, thereby preventing damage to the alveoli. Mutations of the Serpina1 gene can lead to reduced serum levels of AAT and decreased protein functionality, allowing for unrestricted elastin breakdown, pulmonary inflammation and eventual emphysema. See, e.g., 1: Lomas et al., J Hepatol. 2016 Mar. 28. pii: S0168-8278(16)30083-6; Strange et al., Semin Respir Crit Care Med. 2015 August; 36(4):470-7; Traclet et al., Rev Mal Respir. 2015 April; 32(4):435-46; Teschler, Eur Respir Rev. 2015 March; 24(135):46-51; Duvoix et al., Rev Mal Respir. 2014 December; 31(10):992-1002; Stockley, Clin Chest Med. 2014 March; 35(1):39-50).